Relationships between maximal muscle oxidative capacity and blood lactate removal after supramaximal exercise and fatigue indexes in humans

Abstract

The present study investigated whether blood lactate removal after supramaximal exercise and fatigue indexes measured during continuous and intermittent supramaximal exercises are related to the maximal muscle oxidative capacity in humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (gamma(2)), which denoted the blood lactate removal ability. Fatigue indexes were calculated during all-out (FI(AO)) and repeated 10-s cycling sprints (FI(Sprint)). Biopsies were taken from the vastus lateralis muscle, and maximal ADP-stimulated mitochondrial respiration (V(max)) was evaluated in an oxygraph cell on saponin-permeabilized muscle fibers with pyruvate + malate and glutamate + malate as substrates. Significant relationships were found between gamma(2) and pyruvate + malate V(max) (r = 0.60, P < 0.05), gamma(2) and glutamate + malate V(max) (r = 0.66, P < 0.01), and gamma(2) and citrate synthase activity (r = 0.76, P < 0.01). In addition, gamma(2), glutamate + malate V(max), and pyruvate + malate V(max) were related to FI(AO) (gamma(2) - FI(AO): r = 0.85; P < 0.01; glutamate + malate V(max) - FI(AO): r = 0.70, P < 0.01; and pyruvate + malate V(max) - FI(AO): r = 0.63, P < 0.01) and FI(Sprint) (gamma(2) - FI(Sprint): r = 0.74, P < 0.01; glutamate + malate V(max) - FI(Sprint): r = 0.64, P < 0.01; and pyruvate + malate V(max) - FI(Sprint): r = 0.46, P < 0.01). In conclusion, these results suggested that the maximal muscle oxidative capacity was related to blood lactate removal ability after a 1-min all-out test. Moreover, maximal muscle oxidative capacity and blood lactate removal ability were associated with the delay in the fatigue observed during continuous and intermittent supramaximal exercises in well-trained subjects.

Intramyocellular lipid accumulation is associated with permanent relocation ex vivo and in vitro of fatty acid translocase (FAT)/CD36 in obese patients

“…Insulin sensitivity was measured in the fasted state with an IVGTT followed by the minimal model analysis as previously published [21]. A skeletal muscle biopsy of the vastus lateralis was performed as previously described [22,23].…”

“…Mitochondrial respiration Respiratory variables of the total mitochondrial population were analysed in situ on fresh permeabilised skeletal muscle fibres as previously described [22]. Respiration rates were recorded in the presence of pyruvate/malate (10 mmol/l) or palmitoyl-L-carnitine (40 µmol/l).…”

Training-induced improvement in lipid oxidation in type 2 diabetes mellitus is related to alterations in muscle mitochondrial activity. Effect of endurance training in type 2 diabetes

“…Respiratory parameters of the total mitochondrial population were analyzed in situ on fresh skeletal muscle fibres as previously described [19]. Bundles of muscle fibres were manually isolated and saponin-skinned (50 µg/ml saponin for 30 min at 4 °C).…”

Loading of Trained Inspiratory Muscles Speeds Lactate Recovery Kinetics

“…Paragraph Number 1 Recent evidence suggests that the respiratory muscles become net producers of lactate when the work of breathing exceeds a critical threshold level (2,16,40) and that specific training of these muscles reduces their rate of lactate production and / or increases their rate of consumption (2,40 have also been reported during exercise following specific respiratory muscle training (RMT; 23,35,38) suggesting that at moderate levels of pulmonary ventilation the respiratory muscles may become net lactate consumers (10). These findings are surprising given the small muscle mass (approximately 0.5% total body mass) of the respiratory muscles and collectively suggest an important, previously underestimated role for the respiratory muscles in the regulation of whole body lactate kinetics.…”